Worm Breeder's Gazette 10(1): 23

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More on Suppressors of bli-6(mn4) IV

M. Schuyler, B. Herman and A. Burton

In the last C.  elegans Newsletter we reported on the isolation of 
EMS-induced extragenic suppressors of bli-6(mn4), a dominant mutation 
causing blister formation.  Since the time of that report, one of us 
changed her name from Winter to Schuyler and left the laboratory for 
some months before returning to the worm-picking life in general and 
suppressors of bli-6 in particular.  We noted in the last report that 
23 of our suppressors by themselves result in a dumpy phenotype, and 
all of these mutations were assigned to known dpy genes (but mutations 
in some dumpy genes do not suppress bli-6(mn4)).  Here we report some 
progress with those suppressors that do not confer a dumpy phenotype.
We have assigned 16 independent wild-type suppressors to linkage 
groups: eleven to LGII, two to LGIV and three to X.  Although some of 
the suppressors are dominant in the sense that animals of genotype 
sup/+; bli-6(mn4)/+ are non-Bli, in all cases sup/+; bli-6(mn4)/bli- 6(
mn4) animals are Bli (sup/sup; bli-6(mn4)/bli-6(mn4) are non-Bli); 
therefore it is possible to conduct complementation tests among all 
pairs of suppressors.  The three X-linked mutations appear to 
complement all other mutations except each other, but we have also 
seen several examples of noncomplementation of nonallelic mutations, 
as expected from the work of Kusch and Edgar (1986; Genetics 113: 621-
639).  We have so far tentatively assigned three of the mutations to 
known genes, based on both complementation testing and map position.  
For example, the homozygous mn312 mutant is not a roller, but 
mn312/rol-8(sc15); bli-6(mn4) animals were non-Bli (and slight left 
rollers) and gave no Bli recombinants among 4,800 self progeny (rol-8(
sc15) is a recessive suppressor of bli-6(mn4); by contrast rol-1(e91) 
and rol-6(e187) do not suppress).  By similar arguments, we are 
assigning mn309 to dpy-10, despite the fact that by itself it does not 
confer a dumpy phenotype, and we are assigning at least one of the 
LGIV mutations to dpy-4.Kusch and Edgar (C.  elegans Newsletter 9, no. 
1) identified mutation called sc109 as a recessive suppressor of bli-
6(sc16).  Curiously, sc109 does not suppress bli-6(mn4).  (We've 
confirmed that our copy of sc109 does suppress sc16.)  We do not know 
the null phenotype of bli-6.  It does not seem to be wild type, since 
wild-type revertants of mn4 invariably carried extragenic suppressors. 
Revertants of mn4/+ have also not yet yielded anything but extragenic 
suppressors.  We plan to identify deficiencies of bli-6(mn4), which we 
have mapped close to midway between unc-5 and unc-24.Many of the sup; 
bli-6(mn4) stocks show defects in alae, such as breaks in the ridges, 
as viewed by Nomarski microscopy.  One type of disconnection in ridges 
seems to be unique to the X-linked mutations.  The alae and annulae of 
bli-6(mn4) animals seem to be normal.  We have seen some abnormalities 
in annulae of mutants by scanning electron microscopy.